Physiological, Biochemical, and Transcriptome Analyses Reveal the Potential Role of ABA in Dufulin-Induced Tomato Resistance to Tomato Brown Rugose Fruit Virus (ToBRFV)

水杨酸 生物 基因 脱落酸 转录组 过氧化氢酶 超氧化物歧化酶 过氧化物酶 基因表达 烟草花叶病毒 WRKY蛋白质结构域 诱导剂 植物抗病性 免疫系统 转录因子 细胞生物学 信号转导 植物病毒 植物对草食的防御 基因表达调控 病毒 植物 生物化学 转基因番茄 烟草响尾蛇病毒 胡椒粉 植物生理学 遗传学 茄科 防御机制
作者
Jinfeng Wang,Shijun Xing,Tao Li,Peiyan Zhao,Jianwei Guo,Yuqi Xia,Yating Liu,Shibo Wu
出处
期刊:Horticulturae [Multidisciplinary Digital Publishing Institute]
卷期号:12 (1): 60-60
标识
DOI:10.3390/horticulturae12010060
摘要

As an important plant immune inducer, Dufulin has long been thought to enhance plant resistance to multiple plant viruses through activating the salicylic acid (SA) pathway. However, whether this immune inducer responds to tomato brown rugose fruit virus (ToBRFV) infection in the same way remains uncertain. In this study, we systematically analyzed the multiple effects of Dufulin treatment on the physiological, biochemical and gene expression patterns in tomato under ToBRFV infection. The results showed that the application of Dufulin could significantly increase the chlorophyll content; elevate the activities of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT); reduce the ToBRFV viral load; and enhance plant growth. Moreover, we found that Dufulin treatment could increase both SA and abscisic acid (ABA) contents. However, SA-related genes were not strongly activated as the genes involved in ABA biosynthesis and signal transduction pathways. This suggested that ABA likely plays an unrecognized role in the formation of this induced resistance. Through weighted gene co-expression network analysis (WGCNA) and cis-element analysis of the target gene promoters, we identified that SlABI5-like and SlWRKY4 might be the key potential transcription factor genes for Dufulin-induced tomato resistance to ToBRFV, and constructed their molecular regulatory network. We also conducted qRT-PCR assay to verify the gene expression patterns involved in this study. These findings potentially provide new insights into the mechanism of Dufulin-induced antiviral resistance, and enlarge important molecular targets for ToBRFV prevention and control.

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